The promotion of renal-related inflammatory mechanisms occurs through TMAO activating NLRP3 inflammasomes and NF-κB signal transduction, with NF-κB playing a role in the DKD process by promoting vascular inflammation and oxidative stress, becoming a potential pathogenic mechanism in DKD (Huang et al., 2023) (Figure 10A). This evidence concerns the gene NFKB1 and diabetic kidney disease.